Elevated blood pressure in pregnancy is a well recognised complication which can lead to significant morbidity and mortality. It is the most common medical complication of pregnancy.
There are a few important aspects of hypertension in pregnancy to consider. Chronic hypertension - the presence of maternal high blood pressure before 20 weeks gestation, or if the mother is already on antihypertensive agents. Gestational hypertension - new hypertension developing after 20 weeks gestation, but not associated with proteinuria. Preeclampsia - new hypertension developing after 20 weeks gestation associated with significant proteinuria. Severe preeclampsia - preeclampsia with severely elevated BP or organ dysfunction. Eclampsia - seizures with preeclampsia
Hypertension is defined as: Mild - >140/90 mmHg Moderate - >150/100 mmHg Severe - >160/110 mmHg
Significant proteinuria is defined as:
Total 24h protein loss > 300mg
Protein >2+ on 2 seperate urine dipsticks over 4 hours apart
Urine protein creatinine ratio > 30 mg/mmol
Hypertension in Pregnancy
This may include patients who have known hypertension who then become pregnant, or who have hypertension identified during their pregnancy (< 20 weeks). It is different from the preeclampsia spectrum (i.e. isn’t solely related to the placenta) but still imparts increased risk to the mother and foetus.
Women with hypertension in pregnancy are at increased risk of:
There is also an increased risk to the foetus of:
Management Management will depend on the risks of the specific patient of complications. Patients should be reviewed early. Some patients may prefer non-medical management with close observation. Antihypertensive medications should be reviewed, and the risks discussed with patients - this will often involve a change in medications:
ACE inhibitors/AR2B - should be swapped as have an increased rate of congenital abnormalities
Diuretics - should be swapped as may impact on placental blood flow
Return to normal medications can often be instigated after delivery.
BP control should be targeted at <150/100 mmHg. A more aggressive target of <140/90 should be the goal in patients with end-organ damage. The diastolic target shouldn’t be below 80 mmHg (placental perfusion).
Patients should receive regular urine dip screening to check for proteinuria. If this shows detectable protein, further investigation should be performed to assess the extent of protein loss - urine PCR, 24 hour urinary protein.
There should be US assessment of foetal growth at 28-30 and 32-34 weeks.
A.k.a. Pregnancy induced hypertension. These patients need close observation to allow early detection of preeclampsia. Around 40% will go on to develop preeclampsia.
Management Will be guided by the severity of the hypertension.
Preeclampsia is a multisystem disorder of endothelial dysfunction. It is believed to arise from abnormal placental development. Specifically, there is poor trophoblastic invasion. The consequence is that the the maternal spiral arteries, which usually undergo massive dilation, remain fairly narrow. This impairs the blood flow to the placenta and the foetus. The hypoperfusion (and hypoxia) probably results in the production of a number of vasoactive molecules. These subsequently pass into the mother, where their action on the endothelial cells throughout the body produce the multisystem features of the disorder.
The vasospasm/vasoconstriction and endothelial dysfunction in different locations in the mother can be seen to lead to many of the features of the conditions:
There are several recognised risk factors for developing preeclampsia. Maternal:
Age >35 or < 25
Previous history hypertension in pregnancy
Family history of preeclampsia
Obesity (BMI >35)
First pregnancy with new partner
Severe preeclampsia affects about 5 in 1000 pregnancies. Eclampsia affects around 5 in 10,000 pregnancies. Around 44% of seizures actually occur in the postnatal period.
Preeclampsia and its complications are the second highest cause of direct maternal deaths in pregnancy.
Due to the screening in place for hypertension in pregnancy, it is almost always detected whilst asymptomatic. There are a number of ways that severe preeclampsia amy present though:
Visual disturbances e.g. blurred vision, flashing lights
Sudden swelling - face, hands, feet
Abdominal pain - right upper quadrant/epigastric
Nausea and vomiting
There may be worrying clinical signs detectable on examination:
The foetus may also show reduced movements or poor growth.
There may also be a number of biochemical disturbances:
U&Es - deranged, including impaired renal function
LFTs - elevated LFTs, low albumin
FBC - low platelets, haemolysis
Elevated serum urate (>360 micromol/l)
HELLP syndrome refers to the combination of:
Elevated Liver enzymes
Rarely the presentation may be of an acute CVA with focal neurology.
A full assessment is needed. Patients with preeclampsia or severe hypertension should be admitted for this.
A detailed history of the patient’s medical background, with specific focus on this pregnancy is needed. Specific enquiry into the concerning symptoms noted above.
An ABC assessment will be appropriate in patients presenting acutely unwell e.g. eclampsia. Otherwise, a focused examination should aim to elicit any worrying features of severe preeclampsia, as above.
SImilarly, focused investigations will be guided at looking for features of severity or complications:
Urine protein measurement - PCR, 24h collection
Head imaging (CT) is not routinely indicated.
The only ‘cure’ for preeclampsia is delivery of the placenta. As such, the management will involving the balancing of premature delivery against the risks of continuing the pregnancy. In preeclampsia, this will involve close inpatient monitoring of the condition:
BP measurement 4 times/day
Questioning on adverse features (e.g. headache) with each BP reading
Blood test 3 times weekly
Regular foetal monitoring
In uncomplicated preeclampsia, the pregnancy can often be maintained until 34 weeks.
In patients with moderately or severely elevated BP, oral antihypertensives treatment will be commenced:
Target BP is SBP <150 and DBP 80-100 mmHg.
Here the risks of complications are increased. Management arms include:
Delivery of foetus
BP control This will again be focused on reducing the risk of cerebrovascular events in the mother. Target BP control will be as above (SBP <150 and DBP 80-100 mmHg) In severe disease, the need for rapid (but not excessive) control of BP may make oral therapy unsuitable. Intravenous therapy (e.g. labetalol) may provide a better control of BP in this way. Similarly, invasive BP measurement may be indicated to allow detection of excessively rapid changes, and for regular blood tests. Hydralazine is an alternative IV agent for this.
In labour, adequate analgesia (i.e. an effective epidural) is a important way to achieve BP control.
The common drugs are: Labetalol:
IV: Loading 50mg, infusion 20-160mg/hr
Avoid in asthmatics
Oral only: 0.5-3mg/24h in 3 divided doses
May cause haemolysis, postural hypotension, postnatal depression
Oral only: 10mg followed by 10-20mg MR form 8 hourly
Avoid sublingual route (excessive BP drop)
Can cause headache and oedema (similar to signs of severe preeclampsia)
Adverse effects from vasodilation: headache, tachycardia, flushing
Fluid balance The endothelial dysfunction results in significant capillary leakage in many cases. As such, pulmonary oedema remains a significant risk in these patients. As such, a tight fluid balance is important in these patient. The target is on the dry side:
Total fluid input is recommended as no more than 1ml/kg/hr.
Urine output of >0.5ml/kg should still be targeted.
Oliguria is relatively common, but the incidence of significant AKI in this cohort seems low, and the balance of risks favours keeping patients dry. In cases where there is suspected severe intravascular depletion, other methods for assessing volume status should be considered, and cautious fluid therapy considered e.g. 250ml bolus.
Seizure Prophylaxis Eclampsia will complicate 1-2% of cases of preeclampsia. Magnesium sulphate is the treatment of choice for correcting the pathophysiological basis of eclampsia. It is believed that the vasodilatory effects break the vasospasm and reestablish cerebral blood flow, reducing the risk of seizures. Magnesium prophylaxis may be considered in cases of high risk patients as it reduces the risk of development of eclampsia by around 50%.
Magnesium therapy involves:
Loading dose: 4g - made up to 40ml and infused over 10 mins
Maintenance: 1-2g/hr - 5g in 50ml infused at 10-20ml/hr
When given, the infusion should continue for 24 hours after delivery, or the most recent seizure.
As being administered, the patient needs regular clinical assessment. Toxicity can occur, but can often be recognised clinically before adverse features arise.
Target levels 2.0-4.0 mmol/l
ECG changes3.0-5.0 mmol/l
Loss of deep tendon reflexes>5.0 mmol/l
Resp. & CNS depression>7.0 mmol/l
Cardiac arrest >12 mmol/l
Regular clinical assessment should therefore include:
Deep tendon reflexes
Magnesium is excreted renally so Mg2+ levels should be measured if urine output is less than 100ml per 4 hours. Otherwise, routine serum measurement isn’t required.
If deep tendon reflexes are lost or respiratory rate drops, the infusion should be stopped until the changes resolve. Severe adverse features (e.g. respiratory arrest) can be treated with cautious administration of 10ml 10% calcium gluconate.
Delivery of Foetus This will be the definitive treatment. The decisions around delivery will be a balance of risk vs benefit taking into account factors such as current gestation, severity of preeclampsia, resources e.g. neonatal care. In severe cases, if the gestation is beyond 34 week, the risks of prematurity to the foetus are often less significant. If the gestation is below 34 weeks, the risks of neonatal lung immaturity are significant, and there will often be attempts to delay delivery to allow steroids to be administered and optimise the chances for foetal lung maturity. Similarly, the choice of delivery mode will vary on different factors. Patients with preeclampsia may labour and progress rapidly.
Analgesia and anaesthesia options need extra consideration in this scenario. Labour epidural analgesia is often strongly recommended if vaginal delivery is planned. The analgesia can block the significant sympathetic response to the pain of labour, which can lead to significant BP rises. Severe preeclampsia is not a contraindication, but the coagulopathic complications (dropping platelets, coagulopathy) may be. Platelet levels > 100 x 10^9/l are likely safe, but may be possible with values of 80-100, if there are no other haemostatic derangement. This will form part of a risk/benefit decision for each patient.
Regional anaesthesia is preferable for any operative intervention. Again, the benefits here lie with the minimisation of any sympathetic response to surgery, or laryngoscopy. However, again the coagulopathic derangements of preeclampsia may prohibit this (or notably increase the risk). Following spinal anaesthesia, there is often a notbaly reduced need for vasopressors, unlike in normal pregnant patients. Vasopressors e.g. phenylephrine, should therefore be used in much lower doses, due to the increased sensitivity.
General anaesthesia may be needed in some cases, mainly when regional anaesthesia is contraindicated. The additional risks in patients with preeclampsia include:
Exaggerated pressor response to laryngoscopy - risk of intracranial haemorrhage
The sympathetic response to laryngoscopy needs to be obtunded to safely intubate these patients. Pharmacological options include:
Alfentanil - 1-2mg bolus
Magnesium - 0.5-1g bolus
Labetalol - 25-50mg bolus
Similar care needs to be taken on extubation.
Patients should be monitored closely after extubation due to the risk of airway oedema and obstruction. If they have been receiving Mg2+ preoperatively, then this can notably prolong muscle relaxant duration. Monitoring is essential. NSAIDs should be avoided due to the risks of renal and platelet dysfunction.
Postpartum The increased risk will continue into the immediate postpartum period, and ongoing monitoring is needed. The appropriate antihypertensive therapy and fluid balance control will need to continue. Treatment can often be weaned fairly rapidly, but not too rapidly with antihypertensive medications, as this would risk rebound hypertension. Patients are at an increased VTE risk, and usually require pharmacological prophylaxis, if coagulopathic complications haven’t developed.
Women at high risk of preeclampsia should be recommended to take aspirin prophylaxis from 12 weeks gestation (75mg OD). High risk patients include:
Previous hypertension in pregnancy
Or patients with 2 of:
Primiparous (or last pregnancy over 10 years ago
Age over 40
Family history of preeclampsia
BMI > 35
Eclampsia is the development of seizures in preeclampsia and is a medical emergency. The management approach should still employ the ABC principles of assessment and resuscitation. Magnesium is the anticonvulsant of choice (as above). Hypertension should be quickly controlled to reduce the risk of intracranial haemorrhage. Intravenous therapy will be needed. Delivery is the definitive treatment, and attempts to prolong the pregnancy at this time are unlikely to be of any benefit. In some cases vaginal delivery may be possible, but there should be strong consideration given to C-section.
This refers to a specific complication of pregnancy that is usually only present alongside preeclampsia or eclampsia. The name represents the 3 features of the syndrome:
Elevated Liver enzymes
I can occur in around 10-20% of cases of severe preeclampsia. Coagulopathy results in platelet deposition in vessels (low platelets) and the collision of RBCs with these depositions results in haemolysis. There is also periportal hemorrhage and ischaemia with hepatic dysfunction.
Management is essentially the same as preeclampsia:
Transfusion of blood products may be required if indicated due to coagulopathy or anaemia.